p53功能获得性突变通过上调ENTPD5和增强N-糖蛋白折叠促进转移。
p53 gain-of-function mutations promote metastasis via ENTPD5 upregulation and enhanced N-glycoprotein folding.
作者信息
Timofeev Oleg, Stiewe Thorsten
机构信息
Institute of Molecular Oncology, Philipps-University , Marburg, Germany.
出版信息
Mol Cell Oncol. 2017 Feb 3;4(2):e1288678. doi: 10.1080/23723556.2017.1288678. eCollection 2017.
Abstract
Mutations in cancer abolish normal tumor suppressive functions of tumor protein p53 (, best known as p53) and convert it into an oncogene. We recently reported the identification of ectonucleoside triphosphate diphosphohydrolase 5 () as a transcriptional target of mutant p53 that enhances folding of N-glycosylated proteins required for cancer cell migration, invasion, and metastasis.
摘要
癌症中的突变会消除肿瘤蛋白p53（通常称为p53）的正常肿瘤抑制功能，并将其转化为一种癌基因。我们最近报告了已鉴定出胞外核苷三磷酸二磷酸水解酶5（ENTPD5）是突变型p53的转录靶点，该靶点可增强癌细胞迁移、侵袭和转移所需的N-糖基化蛋白的折叠。
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